Toxoplasma gondii primarily invades the central nervous system, causing latent infections. Cysts persist in the host for life and there is currently no effective treatment. T. gondii infects human hosts through contaminated meat, invading the intestinal tissue and leading to changes in the number and composition of the gut microbiota. Since probiotic ingestion modulates intestinal microbiota changes, we hypothesized that intestinal microbiota dysbiosis caused by T. gondii infection would be restored following probiotic supplementation. To this end, we orally infected C57BL/6 mice with 10 T. gondii cysts and administered supplemental probiotics daily. We analyzed the levels of T. gondii B1 gene DNA, indicative of T. gondii infection, in brain tissue. We investigated alterations in the gut microbiota composition and functional pathways between the probiotic and non-probiotic treatment groups via next-generation sequencing analysis of each fecal sample. The infection level in the probiotic-treated group was significantly reduced after 4 weeks (p<0.05). Probiotic supplementation notably changed the gut microbiota after 2 weeks of infection, increasing the relative abundance of Intestinimonas massiliensis and Lawsonibacter asaccharolyticus. Probiotic supplements appear to modulate the gut microbiota, activating functional pathways involved in intestinal short-chain fatty acid production and strengthening the intestinal barrier, thereby impeding T. gondii infection and subsequent proliferation. Our findings provide valuable insights into T. gondii infection control and future study directions.

Toxoplasma gondii primarily invades the central nervous system, causing latent infections. Cysts persist in the host for life and there is currently no effective treatment. T. gondii infects human hosts through contaminated meat, invading the intestinal tissue and leading to changes in the number and composition of the gut microbiota. Since probiotic ingestion modulates intestinal microbiota changes, we hypothesized that intestinal microbiota dysbiosis caused by T. gondii infection would be restored following probiotic supplementation. To this end, we orally infected C57BL/6 mice with 10 T. gondii cysts and administered supplemental probiotics daily. We analyzed the levels of T. gondii B1 gene DNA, indicative of T. gondii infection, in brain tissue. We investigated alterations in the gut microbiota composition and functional pathways between the probiotic and non-probiotic treatment groups via next-generation sequencing analysis of each fecal sample. The infection level in the probiotic-treated group was significantly reduced after 4 weeks (p<0.05). Probiotic supplementation notably changed the gut microbiota after 2 weeks of infection, increasing the relative abundance of Intestinimonas massiliensis and Lawsonibacter asaccharolyticus. Probiotic supplements appear to modulate the gut microbiota, activating functional pathways involved in intestinal short-chain fatty acid production and strengthening the intestinal barrier, thereby impeding T. gondii infection and subsequent proliferation. Our findings provide valuable insights into T. gondii infection control and future study directions.

Toxoplasma gondii primarily invades the central nervous system, causing latent infections. Cysts persist in the host for life and there is currently no effective treatment. T. gondii infects human hosts through contaminated meat, invading the intestinal tissue and leading to changes in the number and composition of the gut microbiota. Since probiotic ingestion modulates intestinal microbiota changes, we hypothesized that intestinal microbiota dysbiosis caused by T. gondii infection would be restored following probiotic supplementation. To this end, we orally infected C57BL/6 mice with 10 T. gondii cysts and administered supplemental probiotics daily. We analyzed the levels of T. gondii B1 gene DNA, indicative of T. gondii infection, in brain tissue. We investigated alterations in the gut microbiota composition and functional pathways between the probiotic and non-probiotic treatment groups via next-generation sequencing analysis of each fecal sample. The infection level in the probiotic-treated group was significantly reduced after 4 weeks (p<0.05). Probiotic supplementation notably changed the gut microbiota after 2 weeks of infection, increasing the relative abundance of Intestinimonas massiliensis and Lawsonibacter asaccharolyticus. Probiotic supplements appear to modulate the gut microbiota, activating functional pathways involved in intestinal short-chain fatty acid production and strengthening the intestinal barrier, thereby impeding T. gondii infection and subsequent proliferation. Our findings provide valuable insights into T. gondii infection control and future study directions.

Toxoplasma gondii primarily invades the central nervous system, causing latent infections. Cysts persist in the host for life and there is currently no effective treatment. T. gondii infects human hosts through contaminated meat, invading the intestinal tissue and leading to changes in the number and composition of the gut microbiota. Since probiotic ingestion modulates intestinal microbiota changes, we hypothesized that intestinal microbiota dysbiosis caused by T. gondii infection would be restored following probiotic supplementation. To this end, we orally infected C57BL/6 mice with 10 T. gondii cysts and administered supplemental probiotics daily. We analyzed the levels of T. gondii B1 gene DNA, indicative of T. gondii infection, in brain tissue. We investigated alterations in the gut microbiota composition and functional pathways between the probiotic and non-probiotic treatment groups via next-generation sequencing analysis of each fecal sample. The infection level in the probiotic-treated group was significantly reduced after 4 weeks (p<0.05). Probiotic supplementation notably changed the gut microbiota after 2 weeks of infection, increasing the relative abundance of Intestinimonas massiliensis and Lawsonibacter asaccharolyticus. Probiotic supplements appear to modulate the gut microbiota, activating functional pathways involved in intestinal short-chain fatty acid production and strengthening the intestinal barrier, thereby impeding T. gondii infection and subsequent proliferation. Our findings provide valuable insights into T. gondii infection control and future study directions.

Toxoplasma gondii primarily invades the central nervous system, causing latent infections. Cysts persist in the host for life and there is currently no effective treatment. T. gondii infects human hosts through contaminated meat, invading the intestinal tissue and leading to changes in the number and composition of the gut microbiota. Since probiotic ingestion modulates intestinal microbiota changes, we hypothesized that intestinal microbiota dysbiosis caused by T. gondii infection would be restored following probiotic supplementation. To this end, we orally infected C57BL/6 mice with 10 T. gondii cysts and administered supplemental probiotics daily. We analyzed the levels of T. gondii B1 gene DNA, indicative of T. gondii infection, in brain tissue. We investigated alterations in the gut microbiota composition and functional pathways between the probiotic and non-probiotic treatment groups via next-generation sequencing analysis of each fecal sample. The infection level in the probiotic-treated group was significantly reduced after 4 weeks (p<0.05). Probiotic supplementation notably changed the gut microbiota after 2 weeks of infection, increasing the relative abundance of Intestinimonas massiliensis and Lawsonibacter asaccharolyticus. Probiotic supplements appear to modulate the gut microbiota, activating functional pathways involved in intestinal short-chain fatty acid production and strengthening the intestinal barrier, thereby impeding T. gondii infection and subsequent proliferation. Our findings provide valuable insights into T. gondii infection control and future study directions.

To figure out the epidemiological status and relevance with other diseases in toxoplasmosis, we checked serum IgG antibody titers of 1,265 patients and medical records of seropositive patients. Seropositive rates were 6.6% by latex agglutination test (LAT) and 6.7% by ELISA. No significant differences were detected between sexes and age groups. The peak seroprevalence was detected in the 40-49-year-old age group. According to clinical department, Toxoplasma-positive rates were high in patients in psychiatry, ophthalmology, health management, emergency medicine, and thoracic surgery. Major coincidental diseases in seropositive cases were malignant neoplasms, diabetes mellitus, arthritis, chronic hepatitis B, chronic renal diseases, schizophrenia, and acute lymphadenitis, in the order of frequency. In particular, some patients with chronic hepatitis B and malignant neoplasms had high antibody titers. These results revealed that the seroprevalence of toxoplasmosis in a general hospital-based study was similar to that in a community-based study, and T. gondii seropositivity may be associated with neoplasms, diabetes, and other chronic infections.
Adolescent ; Adult ; Aged ; Aged, 80 and over ; Animals ; Antibodies, Protozoan/blood ; Child ; Child, Preschool ; Comorbidity ; Female ; Hospitals, General ; Humans ; Immunoglobulin G/blood ; Infant ; Infant, Newborn ; Korea/epidemiology ; Male ; Middle Aged ; Seroepidemiologic Studies ; Toxoplasma/*immunology ; Toxoplasmosis/*epidemiology ; Young Adult

Toxoplasma gondii is an obligate intracellular parasite that stimulates production of high levels of proinflammatory cytokines, which are important for innate immunity. NLRs, i.e., nucleotide-binding oligomerization domain (NOD)-like receptors, play a crucial role as innate immune sensors and form multiprotein complexes called inflammasomes, which mediate caspase-1-dependent processing of pro-IL-1β. To elucidate the role of inflammasome components in T. gondii-infected THP-1 macrophages, we examined inflammasome-related gene expression and mechanisms of inflammasome-regulated cytokine IL-1β secretion. The results revealed a significant upregulation of IL-1β after T. gondii infection. T. gondii infection also upregulated the expression of inflammasome sensors, including NLRP1, NLRP3, NLRC4, NLRP6, NLRP8, NLRP13, AIM2, and NAIP, in a time-dependent manner. The infection also upregulated inflammasome adaptor protein ASC and caspase-1 mRNA levels. From this study, we newly found that T. gondii infection regulates NLRC4, NLRP6, NLRP8, NLRP13, AIM2, and neuronal apoptosis inhibitor protein (NAIP) gene expressions in THP-1 macrophages and that the role of the inflammasome-related genes may be critical for mediating the innate immune responses to T. gondii infection.
Apoptosis ; Cytokines ; Gene Expression ; Immunity, Innate ; Inflammasomes* ; Macrophages* ; Multiprotein Complexes ; Negotiating ; Neurons ; Parasites ; RNA, Messenger ; Toxoplasma* ; Up-Regulation

Fasciola hepatica is a trematode that causes zoonosis mainly in cattle and sheep and occasionally in humans. Fascioliasis has been reported in Korea; however, determining F. hepatica infection in snails has not been done recently. Thus, using PCR, we evaluated the prevalence of F. hepatica infection in snails at 4 large water-dropwort fields. Among 349 examined snails, F. hepatica-specific internal transcribed space 1 (ITS-1) and/or ITS-2 markers were detected in 12 snails and confirmed using sequence analysis. Morphologically, 213 of 349 collected snails were dextral shelled, which is the same aperture as the lymnaeid snail, the vectorial host for F. hepatica. Among the 12 F. hepatica-infected snails, 6 were known first intermediate hosts in Korea (Lymnaea viridis and L. ollula) and the remaining 6 (Lymnaea sp.) were potentially a new first intermediate host in Korea. It has been shown that the overall prevalence of the snails contaminated with F. hepatica in water-dropwort fields was 3.4%; however, the prevalence varied among the fields. This is the first study to estimate the prevalence of F. hepatica infection using the vectorial capacity of the snails in Korea.
Animals ; Base Sequence ; DNA, Helminth/chemistry/genetics ; DNA, Ribosomal Spacer/chemistry/genetics ; Fasciola hepatica/anatomy & histology/genetics/*isolation & purification ; Molecular Sequence Data ; Oenanthe/growth & development ; *Polymerase Chain Reaction ; Republic of Korea ; Sequence Analysis, DNA ; Snails/growth & development/*parasitology

Trichomonas vaginalis induces proinflammation in cervicovaginal mucosal epithelium. To investigate the signaling pathways in TNF-alpha production in cervical mucosal epithelium after T. vaginalis infection, the phosphorylation of PI3K/AKT and MAPK pathways were evaluated in T. vaginalis-infected SiHa cells in the presence and absence of specific inhibitors. T. vaginalis increased TNF-alpha production in SiHa cells, in a parasite burden-dependent and incubation time-dependent manner. In T. vaginalis-infected SiHa cells, AKT, ERK1/2, p38 MAPK, and JNK were phosphorylated from 1 hr after infection; however, the phosphorylation patterns were different from each other. After pretreatment with inhibitors of the PI3K/AKT and MAPK pathways, TNF-alpha production was significantly decreased compared to the control; however, TNF-alpha reduction patterns were different depending on the type of PI3K/MAPK inhibitors. TNF-alpha production was reduced in a dose-dependent manner by treatment with wortmannin and PD98059, whereas it was increased by SP600125. These data suggested that PI3K/AKT and MAPK signaling pathways are important in regulation of TNF-alpha production in cervical mucosal epithelial SiHa cells. However, activation patterns of each pathway were different from the types of PI3K/MAPK pathways.
Cell Line ; Cervix Uteri/enzymology/metabolism/*parasitology ; Epithelial Cells/*enzymology/metabolism/parasitology ; Female ; Humans ; *MAP Kinase Signaling System ; Mucous Membrane/*enzymology/metabolism/parasitology ; Phosphatidylinositol 3-Kinases/genetics/*metabolism ; Proto-Oncogene Proteins c-akt/genetics/*metabolism ; Trichomonas Vaginitis/*enzymology/genetics/metabolism/parasitology ; Trichomonas vaginalis/*physiology ; Tumor Necrosis Factor-alpha/genetics/*metabolism

We studied on the proteomic characteristics of Toxoplasma gondii KI-1 tachyzoites which were originally isolated from a Korean patient, and compared with those of the well-known virulent RH strain using 2-dimensional electrophoresis (2-DE), mass spectrometry, and quantitative real-time PCR. Two-dimensional separation of the total proteins isolated from KI-1 tachyzoites revealed up to 150 spots, of which 121 were consistent with those of RH tachyzoites. Of the remaining 29 spots, 14 showed greater than 5-fold difference in density between the KI-1 and RH tachyzoites at a pH of 5.0-8.0. Among the 14 spots, 5 from the KI-1 isolate and 7 from the RH strain were identified using MALDI-TOF mass spectrometry and database searches. The spots from the KI-1 tachyzoites were dense granule proteins (GRA 2, 3, 6, and 7), hypoxanthine-guanine-xanthine phosphoribosyltransferase (HGRPTase), and uracil phosphoribosyltransferase (UPRTase). The spots from the RH strain were surface antigen 1 (SAG 1), L-lactate dehydrogenase (LDH), actin, chorismate synthase, peroximal catalase, hexokinase, bifunctional dihydrofolate reductase-thymidylate synthase (DHTR-TS), and nucleoside-triphosphatases (NTPases). Quantitative real-time PCR supported our mass spectrometric results by showing the elevated expression of the genes encoding GRA 2, 3, and 6 and UPRTase in the KI-1 tachyzoites and those encoding GRA 7, SAG 1, NTPase, and chorismate synthase in the RH tachyzoites. These observations demonstrate that the protein compositions of KI-1 and RH tachyzoites are similar but differential protein expression is involved in virulence.
Electrophoresis, Gel, Two-Dimensional ; Gene Expression Regulation, Developmental ; Humans ; Molecular Sequence Data ; *Proteomics ; Protozoan Proteins/chemistry/*genetics/metabolism ; Toxoplasma/chemistry/*genetics/*growth & development/metabolism ; Toxoplasmosis/parasitology